Stimulation of Renin by Acute Selective Chloride Depletion in the Rat

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Abstract

SUMMARY

To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 M NaHCOi or 0.15 M NaNOi. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRAi) and 105 minutes after (PRAi) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [121"I]albumin. In experiment 1, rats were prepared on a normal diet. PRAi (7.0 ± 1.0 ng/ml per hr, mean ± SEM) was increased (P <0.05) over PRA, (4.7 ± 0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRAi = o.3 ± 0.7, PRAi - 0.1 ± 0.7, P - NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 weeks on a low salt diet. PRAi (47 ± 5 ng/ml per hr) was increased as compared to PRAi (24 ± 2 ng/ml per hr, P <0.005) in the Cl-depleted group but not in the control group (PRA, = 24 ± 3, PRAi - 27 ± 6 ng/ml per hr, P - NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2a we infused chloride-depleted rats with three times as much albumin as controls and with KHCOj, 100 mEq/liter. Despite volume expansion and potassium loading, PRA, (41 ± 6 ng/ml per hr) was significantly elevated as compared to PRAi (25 ± 4 ng/ml per hr, P <0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-rtimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO,; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRAi levels again were higher (36 ± 6 ng/ml per hr, P <0.05) as compared to PRAi (23 ± 4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cldepleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release. Ore Res 44: 815-831, 1979

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